Abstract

IntroductionSerum B-type natriuretic peptide (BNP) is frequently elevated after subarachnoid hemorrhage (SAH), but whether this high BNP level is related to transient elevation of left ventricular filling pressure (LVFP) is unknown. However, in patients with preexistent cardiac pathologies, it is impossible to differentiate between BNP elevation caused by chronic cardiac abnormalities and BNP related to acute neurocardiac injury.MethodsAll adult patients with SAH admitted to our intensive care unit were eligible. Patients were excluded for the following reasons: admission >48 hours after aneurysm rupture, pre-existing hypertension, or cardiac disease. Levels of BNP and cardiac troponin Ic were measured daily for 7 days. Echocardiography was performed by a blinded cardiologist on days 1, 2, and 7. Doppler signals from the mitral inflow, tissue Doppler, and the color M-mode–derived flow propagation velocity (FPV) were obtained to assess echo-estimated LVFP.ResultsDuring a 3-year period, sixty-six consecutive patients with SAH were admitted. Thirty one patients were studied. The BNP level was >100 ng/L in 25 patients (80%) during the first 3 days, with a peak on day 2 (median, 126 ng/L) followed by a gradual decrease (median variation days 1 to 7, 70%). All patients had an ejection fraction >50%. Early transmitral velocity/tissue Doppler mitral annular early diastolic velocity was low: 5.4 (± 1.5) on day 1, 5.8 (± 1.2) on day 2, and 5.1 (± 0.9) on day 7. Early transmitral velocity/FPV was also low: 1.27 (± 0.4), 1.25 (± 0.3), and 1.1 (± 0.2) on days 1, 2, and 7, respectively. Cardiac troponin Ic levels ranged from 0 to 3.67 μg/L and were correlated with BNP (r = 0.63, P < 0.01).ConclusionsBNP rises gradually over two days and return to normal within a week after SAH. Its release is associated with myocardial necrosis, but is unrelated to elevated LVFP assessed by echocardiography.

Highlights

  • Introduction SerumB-type natriuretic peptide (BNP) is frequently elevated after subarachnoid hemorrhage (SAH), but whether this high BNP level is related to transient elevation of left ventricular filling pressure (LVFP) is unknown

  • Its release is associated with myocardial necrosis, but is unrelated to elevated LVFP assessed by echocardiography

  • 66 consecutive patients were admitted to our intensive care unit (ICU) with SAH related to a ruptured aneurysm that was documented by angiography

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Summary

Introduction

B-type natriuretic peptide (BNP) is frequently elevated after subarachnoid hemorrhage (SAH), but whether this high BNP level is related to transient elevation of left ventricular filling pressure (LVFP) is unknown. A: late transmitral velocity; ABS: apical ballooning syndrome; BNP: B-type natriuretic peptide; cTi: troponin Ic; DT: deceleration time of E velocity; E: early transmitral velocity; Ea: tissue Doppler imaging early diastolic velocity; ELISA: enzyme-linked immunosorbent assay; FPV: color M-mode-derived flow propagation velocity; ICU: intensive care unit; IVRT: isovolumic relaxation time; LV: left ventricular; LVEF: left ventricular ejection fraction; LVFP: left ventricular filling pressure; PAP: pulmonary artery pressure; PAWP: pulmonary artery wedge pressure; SAH: subarachnoid hemorrhage; WFNS: World Federation of Neurosurgical Societies. A cardiac source of BNP is supported by a recent study demonstrating that cardiac injury and dysfunction occurring early after SAH are associated with elevated plasma BNP levels [10]

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